Exam one Flashcards
(330 cards)
1
Q
What is the difference between drugs and poisons?
A
the dose
2
Q
What are xenobiotics?
A
foreign chemicals the body doesn’t produce (ex: drugs and poisons)
3
Q
What is a poison/toxicant?
A
any substance that when introduced to body can interfere with life processes or biological functions
4
Q
How is toxicity measured in mammals?
A
LD50 in mg/kg body weight
5
Q
How is toxicity measured in birds?
A
LC50 in mg/kg feed
6
Q
How is toxicity measured in fish?
A
LC50 in mg/L h20
7
Q
What is acute toxicity?
A
effect of a single dose or multiple doses within 24 hours
8
Q
What is subacute toxicity?
A
effect of daily exposure from 1-30days
9
Q
What is chronic toxicity?
A
daily exposure for 3 months or more
10
Q
What is the chronicity factor?
A
ratio between acute LD50 and chronic LD50
11
Q
What is the highest nontoxic dose?
A
largest dose that does not result in undesirable alterations - similar to maximum tolerated dose or minimal toxic dose
12
Q
What is the toxic dose low?
A
lowest dose that produces toxic alterations but administering twice does not result in death
13
Q
What is the toxic dose high?
A
dose that produces toxic alterations and administering twice the dose results in death
14
Q
What is the no effect level?
A
amount of chemical that can be ingested without causing any deaths or illness for any animals in stated period
15
Q
What is LD0?
A
highest dose that does not cause death
16
Q
What is LD50?
A
dose that kills 50% of animals in group
17
Q
What is LD100?
A
lowest dose that kills all animals in a group
18
Q
How do you measure therapeutic index?
A
LD50/ED50 smaller value > smaller safety margin
19
Q
What are the most important routes of toxins?
A
oral, dermal, inhalation
20
Q
What is lethal synthesis? Examples?
A
when the metabolite is more toxic than parent compound ex: organophosphate, ethylene glycol
21
Q
What is the most efficient barrier in the body? Least?
A
most = BBB least = placenta
22
Q
Who assesses drugs?
A
FDA
23
Q
Who assesses chemicals?
A
EPA
24
Q
What is the equation for the standard safety margin?
A
(LD1/SD99 - 1) x 100
25
What is the most important aspect when dealing with toxicosis?
accurate or confirmed diagnosis
26
What are the criteria of diagnosis?
case history, clinical signs, postmortem findings, chemical analysis, lab animal tests
27
What drugs are used to induce emesis when indicated?
syrup of ipecac (1/2-2tsp) or hydrogen peroxide 3% (1-2ml/kg)
28
What are the 4 steps of the treatment of toxicosis?
1. supportive/symptomatic treatment
2. removal of poison
3. specific/antidotal treatment
4. observation
29
What is the best supportive treatment for respiration?
tracheostomy and artificial respiration
30
What can be given as a bronchodilator?
aminophilline
31
What is the supportive treatment for the cardiovascular system?
blood/plasma transfusion, fluids for hypovolemia, cardiac stimulants
32
What drugs can be given as cardiac stimulants?
10% calcium gluconate IV, glucagon IV, digoxin IV
33
What is the best treatment for acidosis?
sodium bicarb IV, 1/6 molar sodium lactate, lactated ringers
34
What is the best treatment for alkalosis?
normal saline IV followed by ammonium chloride PO
35
What is the best treatment for pain?
opioids (fentanyl)
36
What is the best treatment for CNS depression?
artificial respiration
37
What is the best treatment for CNS stimulation?
anticonvulsants - diazepam, propoflo, phenobarb
38
When are emetics used?
within 1-2 hours of ingestion of the poison
39
What are contraindications of emetics?
unconsciousness, corrosives (bleach), petroleum products, dehydration, convulsions
40
What is the DOC for emesis in the dog?
apomorphine
41
What is the antidote for apomorphine?
naloxone IV of levallorphan
42
What is the DOC for emesis in cats?
xylazine
43
What are some other choices of emetics?
syrup of epilac, fresh ground mustard, saturated solution of sodium chloride, hydrogen peroxide
44
What is gastric lavage?
in unconscious ar anesthetized animals, use stomach or ET tube and flush with water and activated charcoal
45
What is enterogastric lavage?
combination of stomach tube and enema
46
What are the purgatives?
sodium sulfate, magnesium sulfate, mineral oil
47
What is used for precipitation?
chemicals that bind the toxicant
48
What is the precipitant for lead?
sulfate
49
What is the precipitant for oxalate?
calcium
50
What is the precipitant for alkaloids?
tannic acid
51
What is the adsorbent of choice?
activated charcoal
52
What kind of charcoal is most effective?
plant in small particle size
53
What is charcoal NOT effective for?
ethanol, methanol, heavy metal salts, fuoride, iodides, nitrate,nitrite, sodium chloride, bleach, fertilizer
54
What drug decreases the effectiveness of charcoal?
ipecac
55
What are the most commonly used diuretics?
mannitol (safer) and furosemide
56
What must be monitored before using diuretics and fluids to enhance elimination?
ensure renal function and hydration of animal
57
What are examples of urinary acidifiers?
ammonium chloride, methionine
58
What do urinary acidifiers help excrete?
weak basic drugs ex: alkaloids, amphetamines
59
What are examples of urinary alkalinizes?
sodium bicarbonate
60
What do urinary alkalinizes help excrete?
weak acidic drugs ex: NSAIDS, phenobarb
61
kg > lb
1 kg = 2.2 lb
62
gal > L > mL
1gal = 4L = 4000mL
63
qt > L > mL > oz
1qt = 1L = 1000mL = 32oz
64
pt > mL > oz
1pt = 500mL = 16oz
65
oz > g
1oz = 30g
66
fl oz > mL
1 fl oz = 30mL
67
gr > mg
1gr = 65 or 60mg
68
m > drop
1m = 1 drop
69
cup > mL > oz
1 cup = 250mL = 8oz
70
T > t > mL
1T = 3t = 15mL
71
t > mL
1t = 5mL
72
What are the organophosphates?
names that have derivatives of word "phosphorus"
73
What is the source of organophosphates?
empty pesticide containers, spraying of infectious agents, contaminated feed or drinking water
74
What is the difference between organophosphates with direct AChE and those without?
those without must be desulfurated before becoming active
75
How long do organophosphates persist in the environment?
not long 2-4 weeks, can penetrate waxy coatings or skin and live longer
76
What is storage activation of organophosphates?
become active and more toxic if sealed and stored 1-2years
77
What are the toxicokinetics of organophosphates?
lipophillic, crosses membranes easily, can absorb through skin or GI or inhaled, well distributed throughout body, enters CNS, no tissue accumulation, tolerance
78
Which organophosphate is more lipophilic and can sequester in fat and stay in body longer?
dichlorvos
79
What is lethal synthesis?
when metabolites are more toxic than original compound
80
Which age of animals are less effected by lethal synthesis?
young animals
81
What is the MOA of organophosphates?
irreversible inhibition of cholinesterase's - non-competitive - increases ACh at all cholinergic sites
82
What is the cause of death in high exposure of organophsphates?
respiratory failure (paralysis), delayed neurotoxicity
83
What is the onset of action for organophosphates?
rapid 15mins - 1hour
84
What are the acute clinical sigs of organophosphate toxicity?
muscarinic stimulation, nicotinic stimulation, CNS stimulation, nicotinic blockade > paralysis, coma, dyspnea, death
85
What is organophosphate induced intermediate syndrome?
with massive doses (malicious) don't see the initial muscarinic signs and jump right to nicotinic and CNS stimulation
86
What is organophosphate induced delayed polyneuropathy?
peripheral neurotoxicity after surviving acute poisoning - see muscle weakness, ataxia, 10-14 days after exposure
87
What is seen on pathology in organophosphate toxicity?
nonspecific lesions - pulmonary edema, hemorrhage, necrosis of skeletal muscle, pancreatitis
88
How do you test for organophosphates?
stomach/rumen contents, skin from dermal exposure NOT liver/kidney because metabolism is rapid - or look at ACh activity in blood
89
How do you diagnose organophosphate toxicity?
history of exposure, clinical signs, +/- lab testing, atropine response test (if strong response, probably NOT OP)
90
What are the DDX for organophosphate poisoning?
pyrethrins, tremorgenic mycotoxins, amitraz toxicosis, blue-green algae, muscarinic mushrooms
91
How do you treat organophosphate toxicity?
induce emesis (NOT if depressed or seizures), wash with soap water, activated charcoal, supportive care
92
What should be avoided when treating for organophosphate toxicity?
phenothiazines, aminoglycosides, muscle relaxants, drugs that depress respiration (opioids)
93
What drugs are used for organophosphate toxicity?
atropine, 2-PAM
94
What is the antidote for OP toxicity?
2-PAM, pralidoxime, protopam - may not be effective if aging has occurred or against all OP
95
How do you treat intermediate syndrome in OP?
supportive care, 2-PAM, may last for weeks
96
How do you treat OP-induced delayed polyneuropathy?
symptomatic therapy only
97
What is the prognosis for organophosphate toxicity?
lots of factors, mild to moderate generally treatable, acute cases responding to treatment can recover w.i 24 hrs
98
What are the carbamates?
names contain 'carb'
99
Do carbamates undergo storage activation?
NO
100
What are the pharmacokinetics of carbamates?
does NOT require hepatic bioactivation, more toxic in young patients, fast onset, short duration, low exposure can recover w/o tx, metabolized rapidly
101
What is the MOA of carbamates?
reversible inhibition of acetylcholinesterase
102
When does toxicity occur in carbamates?
when carbamylation >> hydrolysis
103
How do you diagnose carbamate toxicity?
measure cholinesterase levels but can give false results since reversible, also not detectable in tissues, blood secretions due to rapid metabolism
104
What is the treatment for carbamates?
atropine, 2-PAM although not reliable
105
In what carbamate is 2-PAM contraindicated?
carbaryl, can increase carbamylation process
106
What are the chlorinated hydrocarbons (organochlorines)?
diphenol aliphatics, aryl hydrocarbons, cyclodienes
107
When were chlorinated hydrocarbons started?
DDT to control disease vectors, lindane for lice in humans
108
Are chlorinated hydrocarbons lipophillic or non-lipophillic?
HIGHLY lipophillic --> bioaccumulation in food chain, residues in tissues, persistent in environment
109
How long do chlorinated hydrocarbons live in the environment?
2-15YEARS
110
What is the toxicity of chlorinated hydrocarbons like?
low toxicity to mammals, cats most sensitive but all animals susceptible
111
How are chlorinated hydrocarbons absorbed?
readily absorbed, distributed everywhere
112
How are chlorinated hydrocarbons excreted?
milk, feces, urine, bile (can be reabsorbed)
113
How does fat effect the TK of chlorinated hydrocarbons?
acts as a sink, keeps it then redistributes after weeks, months - weight loss can disrupt equilibrium
114
Because of the biliary excretion, what is a good treatment for chlorinated hydrocarbons?
activated charcoal
115
What is the MOA of chlorinated hydrocarbons?
Na influx and K efflux in peripheral nerves > partial depolarization of brain> repetitive firing of neuron > axonal hyperactivity
116
What are the clinical signs of chlorinated hydrocarbon toxicity?
CNS stimulation, repetitive firing, weakness, tremors, spastic gait, seizures
117
What species shows different clinical signs of chlorinated hydrocarbon toxicity?
birds show CNS depression and blindness
118
How do you diagnose chlorinated hydrocarbon toxicity?
chemical analysis find in liver, blood or brain in high concentrations - high in fat is not conclusive, no pathognomotic lesions
119
What is the antidote for chlorinated hydrocarbons?
NONE
120
How do you treat chlorinated hydrocarbon toxicity?
emesis, wash with soap, activated charcoal, IV lipid therapy, diazepam for seizures, oxygen, fluids
121
What is the concern about chlorinated hydrocarbons in wildlife?
bioaccumulation and biomagnification, embryo toxicity, thinning eggshells, toxic to aquatics
122
What are pyrethrins?
extract from flowers - chrysanthemums, also used as an insecticide
123
What are pyrethroids
synthetic analog of pyrethrins
124
How long do pyrethrins last in the environment?
NOT long, unstable in air and light
125
What is different between the 1st and 2nd generation pyrethroids?
gen 1 do NOT have alpha-cyano moiety = less potent
126
What is the toxicity of pyrethrins like to mammals?
low, no subacute or chronic forms
127
What species are pyrethrins very toxic to?
fish and some birds - cats more than dogs
128
Are pyrethrins lipid soluble or non-lipid soluble?
lipid soluble
129
Where are pyrethrins metabolized?
GIT, plasma and liver - RAPIDLY
130
Do pyrethrins accumulate in tissues?
NO - no residual effect
131
How does piperonyl but oxide effect pyrethrins?
inhibits metabolism
132
What is the MOA of pyrethrins?
delay closure of Na ion channels in axonal membrane of insect, inhibits ATPase leads to repetitive firing
133
What is the knockdown effect?
rapid paralysis caused by inhibition of neurons -> insect immobile but not dead
134
What type of pyrethroids have a greater effect?
type 2
135
Why do pyrethroids effect insects more than mammals?
work better at lower temp, insect Na channels more sensitive and recover slower, insects have slower metabolism
136
What are some clinical signs of pyrethrin toxicity?
muscle tremors, fine tremors instead of convulsions, depression, ataxia, GI signs, dyspnea, death
137
How do you diagnose pyrethrins?
no specific lesions, toxins ID in liver and brain, clinical signs with history
138
What is the antidote for pyrethrins?
NONE
139
How do you treat pyrethrin toxicity?
wash off, control temp - NO activated charcoal or phenothiazines, treat symptoms, IV lipid therapy
140
What drug can be given to control muscle tremors in pyrethrin toxicity?
methocarbamol
141
What can help control seizures in pyrethrin toxicity?
diazepam, barbituates, propofol
142
Where did rotenone come from?
roots of tropical plants, used for fishing to kill fish
143
What is rotenone in?
insecticides, home garden supplies, flea/tick treatment, pesticide for chickens, dust on crops
144
What species is rotenone very toxic to?
fish and cold blooded animals - converted to highly toxic metabolites that are absorbed in gills
145
Which mammals are most sensitive to rotenone?
pigs - most mammals converted to non-toxic metabolites
146
What is the absorption of rotenone like?
low and incomplete through GI, inhalation more toxic - fats and oils increase absorption
147
How is rotenone eliminated?
w/i 24hrs in the feces
148
What is the MOA of rotenone?
blocks TCA cycle - therefore blocks production of ATP, free radical formation, also anesthetic effect with nerve axons
149
What are the clinical signs of rotenone toxicity?
local irritation, depression, convulsions
150
How do you test for rotenone?
look for compound in stomach contents, feces, urine, history
151
How do you treat rotenone toxicity?
no treatment - supportive tx
152
What are the sources of D-Limonene?
OTC lice, flea, tick products, essential oil, food fragrant
153
What is the toxicity of D-Limonene like?
dogs and cats susceptible, cats > dogs
154
How well is D-Limonene absorbed?
lipid soluble - readily absorbed through GI and skin, wide distribution
155
What are the clinical signs of D-Limonene toxicity?
ataxia, weakness, paralysis, CNS depression, smell like lemons
156
How do you diagnose D-Limonene toxicity?
exposure history
157
How do you treat D-Liminene toxicity?
wash out, monitor temperature
158
Where does nicotine come from?
alkaloid from dried leaves of nicotiana tabacum, nicotine sulfate is also a plant insecticide
159
What is the LD50 of nicotine in dogs?
9.2mg - most nicotine products (cigarettes, cigars, patches etc) have a lot above that
160
How well is nicotine absorbed?
well by inhalation and skin contact but poorly from ingestion unless stomach is alkaline
161
How is nicotine excreted?
bile and urine
162
What is the MOA of nicotine?
mimics ACh and stimulates post-synaptic nicotinic receptors, stimulates CRTZ, can block at high doses
163
What are some clinical signs of nicotine toxicity?
ataxia, hypersalivation, bradycardia, tremors, CNS depression, paralysis of reps muscles > death
164
How do you diagnose nicotine poisoning?
contents in urine, stomach, kidney, liver, blood - history
165
How do you treat nicotine toxicity?
emesis, activated charcoal, acidify urine, fluids, NO antacids, atropine, control seizures
166
What drug is a nonselective nicotinic antagonist used to curb tobacco addiction in humans?
mecamylamine
167
What is amitraz used for?
preventic collars, swine insecticide, plant insecticide
168
What species are amitraz products contraindicated in?
cats and horses
169
What is the acute oral LD50 of amitraz for dogs?
100-150mg/kg
170
What can increase the toxicity of amitraz?
meperidine, sympathomimetic amines, stress
171
How is amitraz absorbed?
PO, inhalation, skin
172
What is the distribution of amitraz?
throughout body including CNS
173
What is the MOA of amitraz?
A2 adrenergic agonist in CNS, A1 and A2 adrenergic agonist in the ANS, MAO inhibitor
174
What are the clinical signs of amitraz toxicity?
bradycardia, ataxia, CNS depression, hypothermia, V/D, cardiovascular collapse, respiratory failure
175
How do you diagnose amitraz toxicity?
chemical analysis of organs, hyperglycemia, history, clinical signs
176
What are the DDX for amitraz toxicity?
cholinesterase inhibitors, pyrethrins
177
What is the antidote for amitraz toxicity?
A2 antagonists: yohimbine, atipamezole
178
What are the treatment methods for amitraz toxicity?
washing, emesis, activated charcoal, cathartics, supportive care, antidote
179
What is DEET used for?
insect repellant for mosquitos, flies and ticks
180
What species are susceptible to DEET toxicity?
cats > dogs, young animals more sensitive
181
How is DEET absorbed?
in skin, accumulates and persists
182
What is the MOA of DEET?
unknown but causes surface irritation
183
What are the clinical signs of DEET toxicity?
depression or excitation, ataxia, tremors, seizurees, hypersalivation, vomiting
184
How do you diagnose DEET toxicity?
20ppm findings in body contents, history, clinical presentation
185
What is the antidote for DEET toxicity?
none!
186
How do you treat DEET toxicity?
wash, emesis, activated charcoal, treat symptoms
187
What is naphthalene found in?
mothballs, organochlorine insecticide
188
What species are susceptible to naphthalene toxicity?
cats > dogs
189
How is naphthalene absorbed?
PO, inhalation and oils from skin can absorb
190
What is the MOA of naphthalene?
irritant, oxidation products cause methemoglobinemia and hemolysis > tissue hypoxia
191
What are the clinical signs of naphthalene toxicity?
mothball breath, salivation, vomiting, diarrhea, hemolysis, heinz bodies, methemoglobinemia, seizures
192
How do you diagnose naphthalene toxicity?
hematologic changes - must differentiate from other causes of RBC oxidative injury, measure levels in blood
193
What is the treatment for naphthalene?
ascorbic acid, methylene blue - emesis, sodium bicarb, supportive care
194
What is ivermectin in?
a macrocytic lactone, endectocide for heartworm and other parasites
195
What species are prone to ivermectin toxicity?
dogs, small birds, collies especially
196
How is ivermectin absorbed?
PO and excreted unchanged in feces
197
What is the half life of ivermectin?
2 days - go with 5x that to get out of system!
198
What is the MDR1 gene mutation?
lack of the MDR1 gene > 50x concentration of drug in the CNS
199
What is the MOA of ivermectin?
GABA agonist
200
What are the clinical signs of ivermectin toxicity?
CNS depression, ataxia, hypersalivation, coma,
201
How do you diagnose ivermectin toxicity?
chemical analysis, history, clinical presentation
202
What is the antidote for ivermectin?
none
203
How do you treat ivermectin toxicity?
emesis, activated charcoal, picrotoxin, physostigmine, supportive care
204
What are the 1st generation anticoagulant rodenticides?
warfarin, pindone, chlorophacinone
205
What are the second generation anticoagulant rodenticides?
brodifacoum, diphacinone, bromodialone
206
What are the second generation anticoagulant rodenticides used for?
pesticides, baits, powders mixed with food maliciously, eating rats/mice that ingested toxic compounds
207
What is secondary toxicosis AKA relay toxicosis?
rat dies from toxin, cat eats rat and is effected by toxin
208
How long do anticoagulant rodenticides last in the environment?
resistant, last weeks to months
209
What are some properties of anticoagulant rodenticides?
odorless and tasteless, action is slow
210
Which generation of anticoagulant is more toxic?
2nd gen effective after one dose, 1st gen more toxic when ingested daily for a week
211
What species are susceptible to anticoagulant rodenticides?
most - pigs, dogs, cats, ruminants, horse, chickens
212
What can enhance toxicosis of anticoagulant rodenticides?
vit K deficiency, liver dz, enzyme inhibitors, drugs that cause hemorrhage, anemia, etc, steroids or thyroxine
213
What decreases toxicity of anticoagulant rodenticides?
pregnancy, lactation, enzyme inducers
214
When do anticoagulant rodenticides reach peak values?
6-12hours
215
Are anticoagulant rodenticides protein bound?
yes, highly bound
216
What is the DOA of anticoagulant rodenticides?
3-4 weeks, long half life
217
Do anticoagulant rodenticides get in milk?
yes, also cross placenta
218
What is the MOA of anticoagulant rodenticides?
inhibit vit K epoxide reductase, depletes reduced vit K, reduced activation of clotting factors 2,7,9,10
219
When is the onset of clinical signs for anticoagulant rodenticides?
1-5 days
220
What are the clinical signs for anticoagulant rodenticide poisoning?
tachypnea, dyspnea, anemia, anorexia, lethargy, hemorrhage, abortion in cattle, death without external evidence of bleeding
221
What are the pathologic lesions associated with anticoagulant rodenticide toxicity?
bleeding, petechiation, bacterial pneumonia
222
What is the chemical analysis for rodenticide toxicity?
detection in blood, coagulation parameters
223
Which test is the earliest indicator of rodenticide toxicity?
PIVKA (sent to lab)
224
What is the treatment for anticoagulant rodenticides?
RBC, FFP, fluids, oxygen, thoracocentesis -
225
How do you know if you need to treat anticoagulant rodenticides with FFP or whole blood?
check PCV <15 give blood
226
What drug is used to treat anticoagulant rodenticide toxicity?
vit K1 PO, bioavailability better after fatty meal, (IV=anaphylaxis, IM=hemmorrhage) won't work for 24 hours, animals in liver failure may not respond
227
Which type of vitamin K is used for anticoagulant rodenticide treatment?
K1 NOT K3
228
When should you recheck the PT in rodenticide poisoning?
Not treating - 36hr and 96hr
| treating - 36hr and 48hr
229
Whats is cholecalciferol used in?
rodenticides, bait, large does of bit D, poisonous plants, human meds/vitamins
230
Which vitamin is CCF?
D3
231
What is the solubility of CCF?
insoluble in H20, soluble in most organic solvent and oil
232
What species are more susceptible to CCF poisoning?
all, young more sensitive
233
Is vit D toxicity acute or chronic?
can be either depending on preparation
234
What are some predisposing factors for CCF toxicity?
renal disease, hyperparathyroid, ingestion of lots of calcium and phosphorus
235
What happens to CCF in the body?
absorbed by GI, binds to serum vitD binding protein, to liver, metabolized to 25 hydroxycholecalciferol (calcidiol) brought to kidney > 1,25 dihydroxycholecalciferol (calcitriol)
236
How is CCF excreted?
bile, feces, milk (toxic levels)
237
What is the MOA of CCF?
increases serum calcium due to increased GI absorption, hyperphosphatemia, deposits calcium in soft tissues
238
What effects does CCF toxicity have?
tissue damage, increased capillary permeability, hemorrhage, loss of sodium and potassium
239
When do clinical signs of CCF toxicity happen?
24-36 hours
240
What are the clinical signs of CCF toxicity?
depends on tissues affected - PU/PD, arrhythmias, vomiting, abdominal pain, muscle twitching, seizures, coma, death
241
What is the main lesion associated with CCF toxicity?
hemorrhagic gastroenteritis
242
What does the lab work look like of an animal with CCF toxicity?
hypercalcemia, hyperphosphatemia, elevated serum 25 hydroxy and 1,25 dihydroxycholecalciferol, decreased iPTH
243
How do you diagnose CCF toxicity?
history, clinical signs, lab, calcification of tissues
244
How do you treat CCF toxicity?
emetics, activated charcoal, saline cathartic, normal saline, furosemide, glucocorticoids, calcitonin, pamidronate disodium, low Ca diet, stay out of sun
245
Where does bromethalin come from?
general use pesticide, bait
246
What animals are sensitive to bromethalin toxicity?
cats > dogs, g-pigs are resistant!
247
How is bromethalin absorbed and distributed?
hgihly lipophilic, absorbed PO, widely distributed, highest in brain and fat
248
What is bromethalin metabolized to?
more toxic metabolite desmethylbromethalin in liver
249
How is bromethalin excreted and what is the half life?
5-6 days, in bile, urine
250
What is the MOA of bromethalin?
uncoupling of oxidative phosphorylation, lack of adequate ATP, insufficient energy for Na/K ion pumps, cerebral and spinal cord edema
251
Which part of the body is the main target in bromethalin poisoning?
brain/CNS
252
When do signs of toxicity occur with bromethalin?
acutely 2-24hrs, subacute 2-3 days
253
What are the clinical signs of bromethalin toxicity?
muscle tremors, hyperthermia, seizures, ataxia, paralysis, hyperreflexia, UMN bladder
254
What lesions are found in bromethalin toxicity?
cerebral edema, diffuse white matter vacuolization in CNS
255
How do you diagnose bromethalin toxicity?
history, clinical signs, brain imaging of white matter vacuolization in CNS, chemical analysis TAT 5-7days
256
What is the antidote for bromethalin toxicity?
none
257
How do you treat bromethalin toxicity?
emetic, activated charcoal, saline cathartic, mannitol, diazepam, supplemental feeding
258
What is strychnine in?
restricted use pesticide to control gophers and squirrels, ingest bait or relay toxicosis
259
What does strychnine come from?
strychnos seeds, bitter taste, poorly water soluble, white powder
260
How long does strychnine live in the environment?
gone from soil w/i 40 days
261
What species are susceptible to strychnine toxicity?
dogs, horses, cattle, pigs > cats
262
What species are resistant to strychnine toxicity?
poultry
263
What can decrease toxicity of strychnine?
committing, food in stomach, small amt over time
264
How is strychnine absorbed?
from GI > crosses BBB > liver
265
How is strychnine eliminated?
urine
266
Is strychnine PP bound?
NO
267
How soon is strychnine eliminated?
w/i 24 hours
268
What is the MOA of strychnine??
blocks postsynaptic effect of inhibitory glycine in spinal cord leading to highly exaggerated reflex arcs
269
When is the onset of strychnine toxicity?
15min - 2hr, rapid death
270
What are the clinical signs of strychnine poisoning?
panting, vomiting, mydriasis, stiffness, muscle twitches, seizures, death by respiratory failure
271
What lab samples can be tested for strychnine poisoning?
urine, stomach contents, liver
272
How do you diagnose strychnine toxicity?
history, clinical signs, lab
273
How do you treat strychnine toxicity?
apomorphine for emesis, gastric lavage, activated charcoal, symptomatic treatment
274
What is contraindicated in the lavage for strychnine toxicity?
sodium bicarbonate, antacids
275
What drugs are used for symptomatic treatments of strychnine poisoning?
pentobarbitol, diazepam, methocarbamol, guaifenesin, xylazine
276
What is zinc phosphate used for?
restricted use pesticides, phosphine gas, baits, poisoned rodents
277
Is zinc phosphate stable in the environment?
stable when dry, decomposes on air or bait w/i 2 weeks, insoluble in H20
278
What type of zinc phosphide leads to acute toxicity?
acute from phosphine gas, chronic from either phosphine gas OR zinc phosphide
279
What enhances zinc phosphide toxicity?
gastric acid - causes hydrolysis of zinc phosphide to phosphine gas at pH 4 or lower
280
How are zinc phosphides absorbed?
in GI tract and inhalation, - GI irritant (skin insignificant)
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how is absorbed phosphine excreted?
lungs , urine
282
What is the MOA of zinc phosphide?
unknown - increases oxygen radicals and direct GI irritation, damage to blood vessels
283
What are the main tissues affected by zinc phosphide toxicity?
brain, heart, kidney, liver, lung
284
What are the clinical signs of zinc phosphide toxicity?
anorexia, vomiting, increased rate and depth of respiration, abdominal pain, bloat, dyspnea, death, CNS stimulation in dogs, yelping and convulsions
285
What is the onset like of zinc phosphide?
rapid - mins to hours
286
Why does death occur in zine phosphide toxicity?
tissue anoxia
287
What are the classic lesions of zinc phosphide toxicity?
odor of rotten fish/garlic, hemorrhagic gastroenteritis, congestion of liver and kidney, pulmonary edema
288
What does the lab work show in zinc phosphide toxicity?
elevated serum zinc, metabolic acidosis
289
How should specimens of zinc phosphide toxicity be contained to send to lab?
rapidly frozen
290
How do you diagnose zinc phosphide toxicity?
history, acetylene odor, clinical signs, rapid onset/death, lab diagnosis
291
Does zinc phosphide pose a risk to hospital staff?
YES! if smelling it at 2ppm (safe limit is 1ppm)
292
What is the antidote for zinc phosphide toxicity?
none
293
What is the treatment for zinc phosphide?
emetics, gastric lavage, PO antacids, activated charcoal, IV fluids, O2, circulatory and pulmonary support,
294
Where does fluoroacetate come from?
called compound 1080, used to control coyotes, and rodents, collar worn by sheep and goats
295
How do animals get fluoroacetate poisoning?
eating poisoned rodents, eating plants that contain fluoroacetate
296
Doe fluoroacetate survive long in the environment?
chemically stable but degraded by soil microorganisms and plant enzymes, odorless and water soluble but insoluble in most organic solvents
297
What species are effected by fluoroacetate toxicity?
dogs > mammals
298
How is fluoroacetate absorbed?
GI tract, lungs, open wounds but NOT intact skin
299
How is fluoroacetate excreted?
in urine
300
What is the MOA of fluoroacetate?
condenses w/ oxaloacetate and competes w citrate for active site of CAC - slows the CAC, decreases respiration and energy, buildup of citrate
301
Which organs are most effected by fluoroacetate toxicity?
brain (ammonia buildup) and heart
302
What are the clinical signs of fluoroacetate toxicity?
rapid onset of GI hyperactivity, CNS stimulation, hyperthermia, heart failure, colic, convulsions
303
What lesions are associated with fluoroacetate toxicity?
rapid rigor mortis, cyanosis, hemorrhages, pulmonary changes, organ congestion
304
What does the lab work show in fluoroacetate toxicity?
elevated citrate, hyperglycemia, metabolic acidosis, ionized hypocalcemia
305
How do you diagnose fluoroacetate toxicity?
history, clinical signs, lesions
306
How do you treat fluoroacetate toxicity?
activated charcoal, with rapid onset tx may not be an option
307
What is the antidote for fluoroacetate toxicity?
acetate
308
What drugs can be given in fluoroacetate poisoning?
calcium chloride for ventricular arrhythmias, sodium bicarb for metabolic acidosis, oxygen, fluids
309
How do animals get water deprivation?
feedining brine, whey or garbage, ingestion of salt licks, drinking water containing salt, overcrowding, frozen water, lack of water, medicated (unpalatable) water
310
What effect does salt have on animals?
taste is attractive, mild irritant to mucous membranes
311
How much salt can animals tolerate in feed?
>10% salt in feed if they have free access to water
312
What species are susceptible to water deprivation?
pigs, cattle and poultry mostly, dogs less
313
How is salt absorbed?
by GI and distributed all over body - enters brain by passive diffusion and removed by active transport
314
How is excess sodium excreted?
in urine, as long as there is enough water
315
What is the MOA of water deprivation?
dehydration increases plasma sodium and cerebral spinal fluid - high sodium in brain inhibits anaerobic glycolysis resulting in lack of energy for active transport
316
What happens with sodium trapped in the brain?
attracts water because of osmotic gradient > cerebral edema and brain damage
317
What are the clinical signs of water deprivation?
early constipation and thirst, vomiting, PU, metabolic acidosis, seizures, circling, head pressing, blindness
318
What lesions are seen in water deprivation that are pathognomonic?
eosinophilic meningoencephalitis is pathognomonic in PIGS ONLY and only within 24 hours of exposure - disappears after
319
What other lesions could be seen with water deprivation?
fluid in body cavities, organ edema, cerebral edema
320
What is used for lab diagnosis of water deprivation?
serum and CSF concentrations, salt in feed
321
How do you diagnose water deprivation?
history, encephalitic signs, lesions and lab diagnosis
322
How do you treat water deprivation?
give small amounts of fresh water - large amount can kill them by causing more cerebral edema, IV fluids, furosemide, anticonvulsants
323
What is the prognosis of water deprivation?
poor, mortality 50%
324
What is the source of acute copper toxicosis?
ingestion of high concentrations of copper - feed additives, in soil
325
Why is acute heavy metal toxicity bad?
very small amount can cause toxicosis, irritants, poor penetrated of membranes, small amount that is absorbed can cause toxicosis because of potency
326
Which heavy metal crosses the BBB and causes CNS damage?
lead
327
What are the clinical signs of acute copper toxicosis?
rapid onset of GI signs, dehydration, shock
328
What species is chronic copper poisoning common in?
sheep > cattle, due to lower maliptinum in sheep that enhance copper toxicosis
329
What is the treatment for acute copper toxicosis?
supportive and symptomatic therapy
330
What enhances excess copper in the body?
molybdenum deficiency
